Basic Sciences: Section 1 Bone Flashcards
Endocrine effects on bone healing:
Cortisone
Negative, decreased callus proliferation
Endocrine effects on bone healing:
Calcitonin
Positive(?), Unknown
Endocrine effects on bone healing:
TH, PTH
Positive, Bone remodeling
Endocrine effects on bone healing:
GH
Positive, increased callus formation
Stages of graft healing
- Inflammation, chemotaxis
- Osteoblast differentiation
- Osteoinduction
- Osteoconduction
- Remodeling, continues for years
Under optimal stability what type of frature healing takes place?
Intramembranous ossification
Under instability what type of frature healing takes place?
Enchondral ossification
Under extreme instability what type of frature healing takes place?
Pseudoarthrosis
Three histologic phases of distraction osteogenesis?
- Latency Phase, 5-7 days, no distraction
- Distraction Phase, 1mm/day, 1 inch/month
- Consolidation Phase, 2x longer than distraction phase
Dietary requirment of Calcium in children?
600 mg/day
Dietary requirment of Calcium in adolescents and young adults (10-25)?
1300mg/day
Mechanism of PTH
- cAMP
- decreased serum calcium stimulates Beta-2 receptors to release PTH.
Mechanism of Calcitonin
- Increased serum Ca cause secretion of Calcitonin by parafollicular clear cells of the thyroid gland
- Controlled by Beta-2 receptors
- Inhibits osteoCLAST resorption
- decreases serum Ca
Hypercalcemia symptoms
- Polyuria
- Polydypsia
- Kidney stones
- Excessive bony resorption
- CNS effects - confusion, stupor, weakness
- Constipation
Primary hyperparathyroidism
- Overproduction of PTH (parathyroid adenoma MC)
- Increased osteoclastic resorption
- High Ca, PTH, Alk phos, and urinary phos
- Low serum phos
- Brown tumors
Pseudohypoparathyroidism (PHP)
- PTH receptor abnormality, PTH has no effect - blocked by cAMP pathway or lack of cofactors (Mg)
- PTH is normal or high
- Low Ca, High Phos
- Genetic disorder
Albrights hereditary osteodystrophy
- Form of pseudohypoparathyroidism
- PTH receptor abnormality
- Short 1st, 4th, 5th metacarpals/tarsals (brachydactyly)
- Exostosis
- Obesity
- MR
Pseudo-pseudohypoparathyroidism
(pseudo-PHP)
- Phenotype of PHP
- PTH response is normal
Renal osteodystrohpy:
High-turnover
- Kidney disease:
- Decreased phosphate excretion –> very high serum Phos –> decrease Ca –> very high PTH –> SECONDARY HYPERPARATHYROIDISM
- Rugger Jersey spine, osteitis fibrosa, amyloidosis
Renal osteodystrohpy:
Low-turnover
- Normal PTH, elevated Ca and normal Phos
- Due to aluminum deposition in bones which
- decreases mineralization of bone
- decreases proliferation of osteoblasts
- impairs release of PTH from parathyroid glands
- Rugger Jersey spine, osteitis fibrosa, amyloidosis
Sustained increase in PTH (secondary hyperparathyroidism) is caused by which mechanisms?
- Diminished renal excretion of Phosphorus
- Hypocalcemia
- Impaired Calcitriol
- Altered control of PTH release
- Skeletal resistance to PTH
Phosphorus retention causes PTH secretion in what three ways?
- Phos binds to serum calcium –> hypocalcemia –> increaed PTH production
- Phos impairs 1-alpha-hydroxylase–> decrease production of active vitamin D–> increase PTH
- Phos direct stimulation of PTH synthesis
Rickets:
Vitamin D deficiency
- Insufficient Vit D in diet/malabsorbtion
- Bone deformities and hypotonia
- Rachitic Rosary (enlarged costochondral junction)
- Wide growth plates
- decrease Ca and Phos
- High PTH and Alk phos
- Physeal widening/cupping on Xray
Rickets:
Vitamin D dependant
- Type I - pseudo-vitamin D deficiency
- Very low active Vit D (1-alpha hydroxylase is defective)
- Osteomalacia
- Type II
- Very high active Vit D (Vit D receptor defective)
- Osteomalacia
- Alopecia
- Poor mineralization
Rickets:
Vitamin D resistent
- AKA hypophosphatemic rickets
- MC form
- Decrease renal tubular phosphate resoprtion –> Phos spilling into urine
- Vit D iis inappropriatly normal
-
Classic triad
- Hypophosphatemia
- Lower limb deformities
- Stunted growth rate
Hypophosphatasia
- Caused by very low alkaline phosphatase
- Bone deformities and hypotonia
- Early loss of teeth
- Osteomalacia
- Elevated urine phosphoethanolamine is diagnostic
Scurvy
- Vitamin C deficiency –> decrease chondroitin sulfate synthesis –> defective collagen
- BLEEDING (gums, effusions, ecchymosis) –> iron def. –> fatigue
- Thin cortices
- Corner sign (metaphyseal clefts)
- Osteopenia
- Widening zone of provisional calcification
Paget’s disease
- Osteoclastic abnormality –> increased bone turnover
- Bone deformities –> fractures, pain, CHF
- “Picture frame vertabrae”
- High serum Alk Phos
- High urinary hydroxyproline levels
- Virus-like inclusion bodies in osteoclasts
- Phases
- Active
- Lytic - osteoclastic bone resorbtion
- Mixed
- Sclerotic - osteoblastic bone formation
- Inactive
- Active
Hyperthyroidism
- Hypermetabolism –> increased bone turnover –> High Ca
- Normal Phos, Alk Phos, Vit D and PTH
- Increased free thryroxin
- Decreased TSH
Vitamin D intoxication
- Vitamin D cross reacts with intestines –> increasd absorption of Ca
- High Ca and very high Vitamin D
- Tachy, tremors
Hypoparathyroidism
- Decreased Ca and increased Phos
- Basal ganglia calcification
- MC cause is iatrogenic
Osteoporosis
- Type I
- postmenopausal
- affects trabecular/cancellous bone
- Type II
- age-related
- affects BOTH cortical and trabecular bone
- Tx with 1000-1500 mg Ca and 400-800 IU of Vit D per day
Idiopathic transient osteoporosis of the hip
- uncommon
- most common in 3rd trimester or pregnancy, can occur in men as well
- localized osteopenia without hx of trauma
- self-limiting, resolves within 6-8 months (this differentiates it from osteonecrosis)
Osteomalacia
- qualitative defect - mineralization issue
- Caused by:
- Vit D deficient diet
- GI disorders of absorbtion
- Renal osteodystrophy
- Drugs
- antacids (contain aluminum)
- Phynytoin
- Alcoholism
- Xrays
- Looser’s zone fractures
Osteogenesis imperfecta
- Glycine substitution in procollagen –> failure of collagen cross-linking –> Type I collagen mutation
Lead poisoning
- Short stature
- Decreased bone density
- Altered chondrocyte response to PTH-related protein and TGF-B
Osteopetrosis
- Marble bone disease
- Impaired osteoclast/chondroclast function (no ruffled border or clear zone) –> failure of bone resorption –> sclerosis and obliteration of the mudullary canal
- Infantile AR form
- more severe, hepatosplenomegaly, aplasastic anemia
- AD “tarda” form
- generalized osteosclerosis, rugger jersey spine
Osteopoikilosis
- Spotted bone disease
- Islands of deep cortical bone appear within the medullary cavity and cancellous bone of the long bones
- hands/feet MC
Osteonecrosis
- Death of bone not caused by infection
- Typically caused by loss of blood supply - Hip MC
- A/w
- Chronic steroid use
- Alcoholism
- Sickle cell disease
- Dysbarism (caisson’s disease)
- Radiation therapy
- Gaucher’s disease
- Histologic chronology
- autolysis of osteocytes and necrotic marrow –> inflammation of invasion of new mesenchymal cells –> new woven bone over top dead trabeculae –> resorption of dead trabeculae –> COLLAPSE (sometimes)
Chandler’s disease
Osteonecrosis of femoral head in adults
Osteochondrosis:
Van Neck’s disease
ischiopubic synchondrosis
4-11 years
Osteochondrosis:
Legg-Calve-Perthes diseaes
Femoral head
4-8 years
Osteochondrosis:
Osgood-Schlatter disease
Tibial tuberosity
11-15 years
Osteochondrosis:
Sinding-Larsen-Johansson syndrome
inferior patella
10-14 years
Osteochondrosis:
Blount’s disease
Proximal tibial epiphysis
1-3 years (infants)
8-15 years (adolescents)
Osteochondrosis:
Sever’s disease
Calcaneus
9-11 years
Osteochondrosis:
Kohler’s disease
Tarsal navicular
3-7 years
Osteochondrosis:
Freiberg’s infarction
Metatarsal head
13-18 years
Osteochondrosis:
Scheurmann’s disease
Discovertebral junction
13-17 years
Osteochondrosis:
Panner’s disease
Capitellum of humerus
5-10 years
Osteochondrosis:
Thiemann’s disease
Phalanges of hand
11-19 years
Osteochondrosis:
Keinbock’s disease
Carpal lunate
20-40 years
